Deficiencies in Stuart (Prower) Factor, Plasma Thromboplastin Component, Prothrombin, and Factor VII, Due to Malabsorption of Vitamin K
GEORGE C. HOFFMAN, M.A., M.B., B. Chir.
Department of Clinical Pathologyand
JAMES S. HEWLETT, M.D.
Department of Hematology
HEMORRHAGIC phenomena occur in the malabsorption syndromes as an infrequent complication,1–5 and are due to the “hypoprothrombinemia” that results from the impaired absorption of fat and the fat-soluble vitamin K from the bowel. More specifically, it has been demonstrated6 that in vitamin K deficiency, regardless of its pathogenesis, not only is the amount of prothrombin decreased, but also the amounts of factor VII (stable factor, serum prothrombin conversion accelerator, proconvertin) and plasma thromboplastin component (PTC, Christmas factor).
This paper describes the blood coagulation defect in a patient7 with idiopathic steatorrhea; in addition to deficiencies of prothrombin, factor VII, and PTC, there was also a deficiency of the Stuart8 (Prower9) clotting factor.
The patient, a 24-year-old white woman, was first examined on March 31, 1958, because of diarrhea and pedal edema of two years' duration, and severe anorexia of one month's duration. In June, 1956, and again in June and September, 1957, she received two units of whole blood because of anemia. After severe bleeding from the uterus and the urinary tract in December, 1957, she received six units of whole blood. For three weeks prior to examination she had persistent, frank, hematuria. Epistaxis and hemoptysis occurred occasionally, and she bruised easily. Excessive bleeding had not occurred in other members of the family.
On physical examination she weighed 115 pounds and appeared to be extremely malnourished. The tongue was red and atrophic. Numerous ecchymoses were present on both arms, and there were splinter hemorrhages beneath the fingernails.